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BIOLOGY CONCEPTS & CONNECTIONS Fourth Edition Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Neil A. Campbell Jane B. Reece Lawrence.

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Presentation on theme: "BIOLOGY CONCEPTS & CONNECTIONS Fourth Edition Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Neil A. Campbell Jane B. Reece Lawrence."— Presentation transcript:

1 BIOLOGY CONCEPTS & CONNECTIONS Fourth Edition Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Neil A. Campbell Jane B. Reece Lawrence G. Mitchell Martha R. Taylor From PowerPoint ® Lectures for Biology: Concepts & Connections CHAPTER 11 The Control of Gene Expression Modules 11.15 – 11.19

2 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings A mutation can change a proto-oncogene into an oncogene –An oncogene causes cells to divide excessively 11.15 Cancer results from mutations in genes that control cell division THE GENETIC BASIS OF CANCER Mutation within the gene Oncogene Multiple copies of the gene Hyperactive growth-stimulating protein in normal amount Normal growth- stimulating protein in excess Gene moved to new DNA locus, under new controls New promoter Normal growth- stimulating protein in excess Proto-oncogene DNA Figure 11.15A

3 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Mutations that inactivate tumor-suppressor genes have similar effects Figure 11.15B Normal growth- inhibiting protein Cell division under control Tumor-suppressor gene Defective, nonfunctioning protein Cell division not under control Mutated tumor-suppressor gene

4 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings 11.16 Oncogene proteins and faulty tumor- suppressor proteins can interfere with normal signal-transduction pathways Mutations of these genes cause malfunction of the pathway

5 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.16A Normal product of ras gene TARGET CELL GROWTH FACTOR Receptor Hyperactive relay protein (product of ras oncogene) issues signals on its own Relay proteins Transcription factor (activated) DNA NUCLEUS Transcription Translation Protein that STIMULATES cell division

6 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Other cancer- causing mutations inhibit the cell’s ability to repair damaged DNA Figure 11.16B GROWTH- INHIBITING FACTOR Receptor Nonfunctional transcription factor (product of faulty p53 tumor-suppressor gene) cannot trigger transcription Relay proteins Transcription factor (activated) Transcription Translation Protein that INHIBITS cell division Normal product of p53 gene Protein absent (cell division not inhibited)

7 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings 11.17 Multiple genetic changes underlie the development of cancer Cancers result from a series of genetic changes in a cell lineage –As in many cancers, the development of colon cancer is gradual Figure 11.17A CELLULAR CHANGES: Colon wall 1 DNA CHANGES: 23 Increased cell division Oncogene activated Growth of polyp Tumor-suppressor gene inactivated Growth of malignant tumor (carcinoma) Second tumor-suppressor gene inactivated

8 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Mutations that lead to cancer may accumulate in a lineage of somatic cells Figure 11.17B Chromosomes 1 mutation 2 mutations 3 mutations 4 mutations Normal cell Malignant cell

9 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings 11.18 Talking about Science: Mary-Claire King discusses mutations that cause breast cancer Figure 11.18 Researchers have gained insight into the genetic basis of breast cancer –Studies have been done of families in which a disease-predisposing mutation is inherited

10 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings 11.19 Connection: Avoiding carcinogens can reduce the risk of cancer Table 11.19 Lifestyle choices can help reduce cancer risk


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